중증근육무력증의 역사 (The History of Myasthenia Gravis)

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초록

Since Willis described ‘fatigable weakness’ in 1672, most physicians consider it as a kind of hysteria due to the inconsistent
fluctuation of symptoms. Erb presented three cases of ‘bulbal palsy’ in the 1870s, and Oppenheim and Hopper
considered myasthenia gravis as a disease similar to curare poisoning and as a disease induced by attack of the motor
centers by intrinsic toxins, respectively. In 1903, Elliot suggested that a ‘chemical substance’ mediates the nerve impulses
at synapse. However, it was not until 1921 that this was demonstrated by Loewi, who provided evidence from the
famous two-frog-hearts experiment. Dale later revealed the substance to be acetylcholine, and he also suggested that
myasthenia gravis is due to a problem with the motor end plate. In 1934, Walker was prompted by the resemblance
between myasthenia gravis and curare poisoning to apply physostigmine, a curare-poisoning antidote, to a patient, which
produced a dramatic result. Since then the use of anticholinesterase inhibitors has been adopted for standard therapeutic
modality. Some prominent surgeons have also applied thymectomy as a surgical modality. The most recent focus of
myasthenia gravis has been immunological. In 1960, Simpson proposed the autoimmune hypothesis, and Chang et al.
showed that snake venom contained a selective antagonist of the nicotinic acetylcholine receptor, α-bungarotoxin. The
immunization of rabbits with acetylcholine receptor purified from the electrical organs of electric eels by Patrick et al.
induced myasthenic symptoms and signs, and these were reversed by acetylcholinesterase inhibitors. The role of the
autoimmune system has led to the introduction of an immunosuppressive modality and plasma exchange to the field of
clinical neurology.

영어초록

Since Willis described ‘fatigable weakness’ in 1672, most physicians consider it as a kind of hysteria due to the inconsistent
fluctuation of symptoms. Erb presented three cases of ‘bulbal palsy’ in the 1870s, and Oppenheim and Hopper
considered myasthenia gravis as a disease similar to curare poisoning and as a disease induced by attack of the motor
centers by intrinsic toxins, respectively. In 1903, Elliot suggested that a ‘chemical substance’ mediates the nerve impulses
at synapse. However, it was not until 1921 that this was demonstrated by Loewi, who provided evidence from the
famous two-frog-hearts experiment. Dale later revealed the substance to be acetylcholine, and he also suggested that
myasthenia gravis is due to a problem with the motor end plate. In 1934, Walker was prompted by the resemblance
between myasthenia gravis and curare poisoning to apply physostigmine, a curare-poisoning antidote, to a patient, which
produced a dramatic result. Since then the use of anticholinesterase inhibitors has been adopted for standard therapeutic
modality. Some prominent surgeons have also applied thymectomy as a surgical modality. The most recent focus of
myasthenia gravis has been immunological. In 1960, Simpson proposed the autoimmune hypothesis, and Chang et al.
showed that snake venom contained a selective antagonist of the nicotinic acetylcholine receptor, α-bungarotoxin. The
immunization of rabbits with acetylcholine receptor purified from the electrical organs of electric eels by Patrick et al.
induced myasthenic symptoms and signs, and these were reversed by acetylcholinesterase inhibitors. The role of the
autoimmune system has led to the introduction of an immunosuppressive modality and plasma exchange to the field of
clinical neurology.

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